Chronic disease of the neonate Flashcards

1
Q

Chronic diseases of the neonate

A

HIE
IVH
BPD

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2
Q

What is HIE?

A

greatest risk of adverse outcome – severe fetal acidosis (pH 6.7)

major neonatal encephalopathies or seizure – due to perinatal events

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3
Q

Fetal hypoxia may be caused by

A

inadequate oxygenation of maternal blood from hypoventilation during anesthesia
low maternal BP from acute blood loss, spinal anesthesia, or compression of vena cava by gravid uterus
uterine tetany – inadequate relaxation of uterus for placental filling
abruption placenta
compression or knotting of cord
placental insufficiency from toxemia

after birth
1_ CHD or severe pulmo disease
2. severe anemia (hemorrhagic or hemolytic disease
3. shock (sepsis, blood loss, IVH)

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4
Q

Pathogenesis of HIE

A

Hypoxia and ischemia&raquo_space; anaerobic metabolism&raquo_space; lactate and inorganic phosphates

Glutamate accumulates in damaged tissue, intracellular edema because of IC Na

Intial response – shnt blood to brain, heart, adrenals

Effects
- congestion and petechiae in pericardium, pleura, thymus, heart, adrenals and meninges

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5
Q

what are the clinical manifestations of HIE?

A

IUGR with increased vascular resistance – 1st indication of fetal hypoxia
variable or late deceleration pattern

at delivery – meconium stained amniotic fluid – fetal distress

depressed, fail to breathe, remain hypotonic or change to hypertonic state

Pallor, cyanosis, periodic breathing with apnea, slow heart rate and unresponsiveness to stimulation – signs of HIE

Cerebral edema develops next 24 hours – profound brainstem depression&raquo_space; during this time seizures may occur

Heart failure and cardiogenic shock, PPHN< RDS, GI perforation , hematuria&raquo_space; associated with asphyxia due to inadequate perfusion

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6
Q

Diagnosis of HIE

A

Diff for seizure – IVH, hypocalcemia, hypoglycemia or CNS infection

Diffusion weighted MRI – imaging of choice

CT scan – limited

UTZ – limited in term

aEEG (amplitude integrated EEG) – who is at risk for long term brain injury

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7
Q

what are the complications of HIE?

A

Ph <6.7 high risk of death and severe neuro impairment

Brain death after HIE
coma unresponsive to pain, auditory or visual stimulation
apnea with PCO2 rising from 40-60mmHg
absence of brain reflexes

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8
Q

what is the treatment of HIE?

A

Cerebral or body systemic therapeutic hypothermia reduces mortality and major neuro impairment (33.5C within 1st 6 hours after birth)

hypothermia decreases rate of apoptosis, suppresses mediators like glutamate

Phenobarbital (DOC)
Loading dose 20mg/kg)
Additional 5-10mg/kg
Maintenance 3-5mg/kg

Monitor vital signs, prevent hypotension, acid base balance

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9
Q

What is IVH?

A

-develops spontaneously, or due to trauma and asphyxia, often with preterm infants (IVH)

-can be assoc with fetal alloimmune thrombocytopenia, cerebral hemorrhage, or porencephalic cyst

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10
Q

What is the pathogenesis of IVH?

A

VLBW infants – IVH and PVL

IVH (preterms) – iccur in the gelatinous subependymal germinal matrix
Immature blood vessels plus poor tissue support

PVL – involves intrauterine and postnatal events
-hypoxia, venous obstruction from IVH, or undetected fetal stress may result in decreased perfusion to the brain, leading to periventricular hemorrhage and necrosis
-risk for PVL increases in infants with IVH or ventriculomegaly

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11
Q

what are the clinical manifestations of IVH?

A

IVH
-deterioration on 2nd or 3rd day of life

-hypotension, apnea, pallor or cyanosis, poor suck, abnormal eye signs, high pitched shrill cry, convulsions, decreased pmuscle tone,

-metabolic acidosis, shock

-decreased hematocrit or failure to rise after transfusion

Grading
Grade 1 – bleeding isolated to subependymal area
Grade 2 – bleeding within ventricle without ventricular dilatation
Grade 3 – IVH with ventricular dilatation
Grade 4 – IVH with Parenchymal hemorrhage

PVL
usually clinically asymptomatic until neuro sequelae of white matter damage become apparent in later infancy – as spastic motor deficits
may be present at birth but occurs later

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12
Q

Diagnosis of IVH

A

Preterms <32 weeks evaluated with routine cranial UTZ to check

Infants <1000gms highest risk, UTZ within 3-7th day of life

Ff up at 36-40 weeks AOG to check for PVL

MRI – more sensitive for evaluation of extensive periventricular injury, more predictive of long term outcome

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13
Q

What are the complications of IVH?

A

Post hemorrhagic hydrocephalus –

Hydrocephalus – 2-4 weeks after

Prognosis
neuro development (CP, mental devt index if <1000gm)

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14
Q

What is the management of IVH?

A

Antenatal steroids – 24-34 weeks at risk for preterm delivery -> decrease risk IVH

Post hemorrhagic hydrocephalus – ventriculoperitoneal shunt insertion

Symptomatic
Seizures – anticonvulsant drugs
Anemia and coagulopathy – PRBC or FFP

Insert VP shunt
Serial LP and ventricular taps – temporizing but not therapuetic

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15
Q

What is BPD?

A

-result of lung injury in infants requiring mech vent and supplemental O2
-interference with lung anatomic maturation
-alveolar collapse and volutrauma from mech vent 🡪 lung injury
-free radicals from O2, immaturity, infection, PDA, malnutrition 🡪 contribute to BOD

new BPD
-BW <1000 gms
-<28 weeks AOG

features in new BPD
alveolar hypoplasia
variable saccular wall fibrosis
minimal airway disease

occurrence indirectly proportional to gestational age

Vit A supplementation in VLBW infants reduces risk of BPD

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16
Q

What are the clinical manifestations of BPD?

A

-no improvement on 3rd or 4th day of ventilation 🡪 increased need for O2 and ventilator support

-RD worsens 🡪 hypoxia, hypercapnia, O2 dependence, R sided heart failure

4 pathologic stages
acute lung injury
exudative bronchiolitis
proliferative bronchiolitis
obliterative fibroproliferative bronchiolitis

Classification (based on need for O2 support)
Severe – need for PPV or >30% O2 at 36 weeks or discharge
Moderate – need for 22-29% O2 at 36 weeks
Mild – need O2 for >28 days but breathing room air at 36 weeks

Severe BPD – prolonged mech vent
gradual weaning

17
Q

Prognosis of BPD

A

-better for neonates >1500gms

mortality – highest in those who are ventilator dependent > 6 mos

-growth failure, psychomotor retardation, parental stress, nephrolithiasis, osteopenia, electrolute imbalance

airway problems – subglottic stenosis, vocal cord paralysis,

cardiac – pul HTN, systemic HTN

18
Q

What is the treatment of BPD?

A

Nutritional support – calories

Fluid restriction

Drugs
-Furosemide with KCl supplementation– for fluid overload, decreases PIE and PVR
-inhaled bronchodilators (albuterol, CV or DV)

Maintenance of oxygenation

Prompt tx of infection

Preventive tx – postnatal Dexamethasone (assoc with HTN, hyperglycemia, GI bleeding and perforation, sepsis, poor weight gain)

19
Q
A